The Role of the Possible Receptors and Intracellular Pathways in Protective Effect of Exogenous Anandamide in Kindling Model of Epilepsy.


Journal

Neurochemical research
ISSN: 1573-6903
Titre abrégé: Neurochem Res
Pays: United States
ID NLM: 7613461

Informations de publication

Date de publication:
May 2022
Historique:
received: 02 08 2021
accepted: 24 12 2021
revised: 01 12 2021
pubmed: 4 2 2022
medline: 1 4 2022
entrez: 3 2 2022
Statut: ppublish

Résumé

In this research, the involvement of CB1 and TRPV1 receptors in the possible protective effects of anandamide were investigated in the kindling model of epilepsy. The basolateral amygdala of the rat brain was chosen to put stimulating electrodes. Semi-rapid kindling was induced by a repetitive sub-threshold stimulation for 5-9 consecutive days. There were seven groups, six of which were kindled and used for drug testing by intracerebroventricular (i.c.v.) microinjection. (i) Sham, (ii) control group received vehicles, (iii) anandamide (AEA; 100 ng/rat), (iv) capsazepine (TRPV1 antagonist; 100 ng/rat), (v) AM251 (CB1 antagonist; 100 ng/rat), (vi) AM251 + anandamide, and (vii) capsazepine + anandamide. The after-discharge duration, seizure duration, and stage five duration were measured in rats. Moreover, the expressions of the extracellular signal-regulated kinase (ERK) and the cAMP responsive element binding (CREB) proteins in the hippocampus were also studied. The anandamide-treated group showed a significant decrease in seizure scores, while no change was shown in seizure scores in the capsazepine- and AM251-treated groups compared with the control group. Co-administrations of either capsazepine + AEA or AM251 + AEA attenuated the protective effect of AEA against seizure. Furthermore, the group received AEA showed a decrease in the expressions of CREB and p-CREB possibly through the activation of the CB1 and TRPV1 receptors. Activation of CB1 and TRPV1 receptors might be involved in AEA anticonvulsant effect in kindling model of epilepsy. This effect could be due to suppression of CREB phosphorylation in hippocampal neurons.

Identifiants

pubmed: 35112235
doi: 10.1007/s11064-021-03517-5
pii: 10.1007/s11064-021-03517-5
doi:

Substances chimiques

Arachidonic Acids 0
Endocannabinoids 0
Polyunsaturated Alkamides 0
Receptor, Cannabinoid, CB1 0
TRPV Cation Channels 0
anandamide UR5G69TJKH

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1226-1242

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Sepideh Khaksar (S)

Department of Plant Sciences, Biological Sciences, Alzahra University, Tehran, Iran.

Mona Salimi (M)

Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.

Hadi Zeinoddini (H)

Department of Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, No. 2660, Vali-e-Asr Ave, 1996835113, Tehran, Iran.

Nima Naderi (N)

Department of Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, No. 2660, Vali-e-Asr Ave, 1996835113, Tehran, Iran. naderi@sbmu.ac.ir.
Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. naderi@sbmu.ac.ir.

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